Macaque model reveals why elderly people with new coronary pneumonia are more sick
Science and Technology Daily (Reporter Zhao Hanbin) Understanding the immunopathological characteristics of the occurrence of new coronary pneumonia is of great significance to the prevention and treatment of new coronary pneumonia.
On November 22, a reporter from the Science and Technology Daily learned from the Kunming Institute of Zoology, Chinese Academy of Sciences, that a study by the institute found the immunopathological mechanism of delayed inflammatory response in the elderly rhesus monkey model with new coronary pneumonia, which may provide treatment for patients with new coronary pneumonia New ideas.
The research results have recently been published in the international journal "Signal Transduction and Targeted Therapy".
Over-response of the immune system is considered to be one of the main pathogenesis of new coronary pneumonia, and primates provide a good model for the dynamic study of the pathological mechanism of new coronary pneumonia.
A previous study by Zheng Yongtang, a researcher from the Kunming Institute of Zoology, Chinese Academy of Sciences, found that Chinese macaques infected by the new coronavirus showed pathological characteristics similar to those of human patients.
However, unlike young rhesus monkeys, which are characterized by rapid immune response and timely decline of inflammatory response, elderly rhesus monkeys show abnormal changes in the delayed outbreak of inflammatory response in lung tissue.
The age-related abnormal immune microenvironment may have formed in the early stage of new coronavirus infection and continue to affect the disease progression of elderly patients.
In order to verify this hypothesis, the team of researcher Zheng Yongtang conducted a more accurate immunopathological study on the Chinese macaque new coronary pneumonia model based on the analysis of multiple immunofluorescence staining quantitative techniques.
Through the analysis of the lung tissues in the early stage of infection, the research team found that the virus infection was not significantly affected by age. The ACE2 positive cells in the lung tissues of the elderly and young monkeys were greatly reduced after the infection, but the ACE2 positive cells of the old rhesus monkeys apoptosis, The level of autophagy and signal pathway activation is more severe than that of young rhesus monkeys.
In addition, after the elderly rhesus monkeys were infected with the new coronavirus, the inflammatory factor secreting cells in the lung tissue increased greatly, which provided the basis for the inflammation outbreak after tissue lesions.
The lung tissue of old rhesus monkeys naturally highly express some cytokines and interferon signal proteins. The immune tolerance caused by inflammatory senescence inactivates the response ability of the immune system, which explains the delayed inflammatory response of the old rhesus monkey model.
The new coronavirus infection specifically induced the accumulation of CXCR3 positive cells in the lung, spleen and peripheral blood of the old rhesus monkeys, which is an age-related systemic pathological feature.
After the elderly rhesus monkeys are infected with the new coronavirus, a large number of CXCR3 positive cells chemotaxis to the infection site due to the compensation effect, which may be one of the mechanisms that cause more severe lung disease in the elderly rhesus monkeys.